The function of neural tissues such as the retina depends upon the presence of normal complements of tissue-specific genes and upon the normal expression of the protein gene products. If these mechanisms fail, hereditary diseases of the retina, such as retinoblastoma or retinitis pigmentosa, will result. We have found that laminin, an important extracellular matrix protein, slows retinoblastoma cell growth and promotes differentiation. Specifically, it switches development from a photoreceptor pathway to a conventional neuronal-like pathway via a low affinity "differentiative" binding activity, which we have called laminin-binding molecule-100 (LBM-100). LBM-100 could have a major effect on early retinal cell development. In parallel, we have developed new techniques to clone and sequence retina-specific genes at a higher efficiency.